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  • Title: Iron metabolism and anaemia in pregnancy.
    Author: Bentley DP.
    Journal: Clin Haematol; 1985 Oct; 14(3):613-28. PubMed ID: 3907911.
    Abstract:
    The mechanism by which anaemia develops in pregnancy is well understood: haemodilution causes a fall in the haemoglobin concentration during the first and second trimesters of normal pregnancies. Negative iron balance throughout pregnancy, particularly in the latter half, may lead to iron deficiency anaemia during the third trimester. The increase in iron demand is required to meet the expansion in maternal haemoglobin mass and to meet the needs of fetal growth. Fetal demand for iron results in a unidirectional flow of iron to the fetus against a concentration gradient regulated by fetal requirements for iron; this iron transfer occurs almost entirely irrespective of maternal iron status. The development of maternal iron deficiency during pregnancy may be detected by monitoring the haemoglobin concentration frequently; values falling to less than 11 g/dl should be regarded as abnormal, but specific red cell changes, such as microcytosis, may be lacking. A diagnosis of iron deficiency can be most conveniently confirmed by the serum ferritin concentration falling to less than 12 micrograms/l. Women at risk from iron deficiency anaemia can therefore be readily identified and corrective treatment instituted prior to the development of severe anaemia. A serum ferritin concentration of less than 50 micrograms/l in early pregnancy is an indication for iron supplements. Women in whom the serum ferritin concentration is greater than 80 micrograms/l at booking are unlikely to require iron supplements during pregnancy. This approach would eliminate the need for routine prophylactic iron therapy, which, in populations enjoying a good nutritional status, can no longer be justified in early pregnancy. Furthermore, any risk to the fetus from severe maternal anaemia would be avoided by prophylaxis and prompt treatment.
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